[Paradoxical increase in glutamatergic synaptic terminations in mild cognitive impairment due to Alzheimer's disease].
Bell
Karen F S
KF
Cuello
A Claudio
AC
D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology / Q000523:psychology*; D000818:Animals; D003072:Cognition Disorders / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D005260:Female; D005625:Frontal Lobe / Q000378:metabolism / Q000473:pathology; D018698:Glutamic Acid / Q000032:analysis*; D006801:Humans; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D008875:Middle Aged; D009419:Nerve Tissue Proteins / Q000032:analysis*; D016501:Neurites / Q000473:pathology; D017729:Presynaptic Terminals / Q000737:chemistry*; D017470:Receptors, Glutamate / Q000032:analysis*; D017661:Receptors, Presynaptic / Q000032:analysis*; D009435:Synaptic Transmission
D009419:Nerve Tissue Proteins; D017470:Receptors, Glutamate; D017661:Receptors, Presynaptic; D018698:Glutamic Acid